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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Colony stimulating factor 1

The protein encoded by this gene is a cytokine that controls the production, differentiation, and function of macrophages. The active form of the protein is found extracellularly as a disulfide-linked homodimer, and is thought to be produced by proteolytic cleavage of membrane-bound precursors. The encoded protein may be involved in development of the placenta. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Sep 2011] (from NCBI)
Top mentioned proteins: CsF, CAN, GM-CSF, FMS, V1a
Papers on M-CSF
DEL1 - a new player in periodontal disease?
Voronov, Toronto, Canada. In Oral Dis, Feb 2016
Osteoblasts (as well as osteocytes and stromal cells) secrete two key molecules, macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor κB ligand (RANKL), which activate the fusion of the mononuclear precursors to form mature multinucleated osteoclasts.
Software-assisted morphometric and phenotype analyses of human peripheral blood monocyte-derived macrophages induced by a microenvironment model of human esophageal squamous cell carcinoma.
Yokozaki et al., Kōbe, Japan. In Pathol Int, Feb 2016
CD14(+) peripheral blood monocytes (PBMos) from healthy donors were treated with M-CSF and with additional IL-4 or TECM exposure.
Rictor is required for optimal bone accrual in response to anti-sclerostin therapy in the mouse.
Long et al., Nanjing, China. In Bone, Feb 2016
Consistent with the fewer osteoclasts in vivo, bone marrow stromal cells (BMSC) from the RiCKO mice expressed less Rankl but normal levels of Opg or M-CSF, and were less effective than the control cells in supporting osteoclastogenesis in vitro.
Multi-analyte profiling in human carotid atherosclerosis uncovers pro-inflammatory macrophage programming in plaques.
Monaco et al., Oxford, United Kingdom. In Thromb Haemost, Feb 2016
The in vitro production of a specific network of mediators was found to be significantly higher in symptomatic than asymptomatic plaques, including: tumour necrosis factor α, interleukin (IL) 1β, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), CCL5, CCL20, CXCL9, matrix metalloproteinase (MMP)-3 and MMP-9.
Cytokines and Blastocyst Hatching.
Madhulika et al., Bengaluru, India. In Am J Reprod Immunol, Jan 2016
Pro-inflammatory (IL-6, LIF, GM-CSF) and anti-inflammatory (IL-11, CSF-1) cytokines improve hatching rates; they modulate proteases (MMPs, tPAs, cathepsins and ISP1).
Impaired differentiation of macrophage lineage cells attenuates bone remodeling and inflammatory angiogenesis in Ndrg1 deficient mice.
Ono et al., Fukuoka, Japan. In Sci Rep, Dec 2015
We observed that serum levels of macrophage colony-stimulating factor (M-CSF) and macrophage-related cytokines were markedly decreased in KO mice.
The role of inflammation in progression of breast cancer: Friend or foe? (Review).
Jones et al., London, United Kingdom. In Int J Oncol, Sep 2015
Recent successes of PD-1 blockade in treating multiple cancers, and new developments with other immune targets such as CTLA-4 and CSF-1 inhibitors, highlight that it is becoming ever more important that we understand the complexity of the immune and inflammatory systems in the development and progression of breast cancer.
Therapeutic targeting of macrophages in lupus nephritis.
Putterman et al., United States. In Discov Med, Jul 2015
The current literature explores targeting macrophages by several different means, including the CSF-1/CSF-1R signaling axis, the CX3CL1/CX3CR1 signaling axis, the CCL2/CCR2 signaling axis, and Bruton's Tyrosine Kinase (BTK), all of which hold promise as targets for future LN treatments.
[The pathogenic role of macrophage in lupus nephritis].
Funauchi et al., In Nihon Rinsho Meneki Gakkai Kaishi, 2014
Deletion of CSF-1 signaling pathway represented more excellent effect in experimental lupus nephritis.
Macrophage IL-10 blocks CD8+ T cell-dependent responses to chemotherapy by suppressing IL-12 expression in intratumoral dendritic cells.
Coussens et al., Portland, United States. In Cancer Cell, 2014
Blockade of colony-stimulating factor-1 (CSF-1) limits macrophage infiltration and improves response of mammary carcinomas to chemotherapy.
Targeting tumor-associated macrophages with anti-CSF-1R antibody reveals a strategy for cancer therapy.
Rüttinger et al., Penzberg, Germany. In Cancer Cell, 2014
The major survival factor for these macrophages is macrophage colony-stimulating factor 1 (CSF-1).
CSF-1R inhibition alters macrophage polarization and blocks glioma progression.
Joyce et al., New York City, United States. In Nat Med, 2013
Macrophages depend on colony stimulating factor-1 (CSF-1) for differentiation and survival.
A clonogenic progenitor with prominent plasmacytoid dendritic cell developmental potential.
Ohteki et al., Tokyo, Japan. In Immunity, 2013
Although both MDPs and CDPs express the macrophage colony stimulating factor (M-CSF) receptor (M-CSFR), the progenitors were confined to a M-CSFR(-) fraction, identified as Lin(-)c-Kit(int/lo)Flt3(+)M-CSFR(-), and expressed high amounts of E2-2 (also known as Tcf4) an essential transcription factor for pDC development.
M-CSF instructs myeloid lineage fate in single haematopoietic stem cells.
Sieweke et al., Marseille, France. In Nature, 2013
Here we show that macrophage colony-stimulating factor (M-CSF, also called CSF1), a myeloid cytokine released during infection and inflammation, can directly induce the myeloid master regulator PU.1 and instruct myeloid cell-fate change in mouse HSCs, independently of selective survival or proliferation.
Osteoclasts: New Insights.
Teitelbaum et al., Birmingham, United States. In Bone Res, 2013
Osteoclasts differentiate from cells of the monocyte/macrophage lineage upon stimulation of two essential factors, the monocyte/macrophage colony stimulating factor (M-CSF) and receptor activation of NF-κB ligand (RANKL).
The CSF-1 receptor ligands IL-34 and CSF-1 exhibit distinct developmental brain expression patterns and regulate neural progenitor cell maintenance and maturation.
Stanley et al., New York City, United States. In Dev Biol, 2012
Postnatal neocortical expression showed that CSF-1 was expressed in layer VI, whereas IL-34 was expressed in the meninges and layers II-V.
Increased expression of macrophage colony-stimulating factor and its receptor in patients with endometriosis.
Tekmal et al., San Antonio, United States. In Fertil Steril, 2012
Suggest that CSF-1 and its receptor, C-FMS, are involved in the genesis of early endometriotic lesions and that endometriotic lesions contribute to elevated CSF-1 levels in the peritoneal fluid of women with endometriosis.
Therapeutic applications of macrophage colony-stimulating factor-1 (CSF-1) and antagonists of CSF-1 receptor (CSF-1R) signaling.
MacDonald et al., Edinburgh, United Kingdom. In Blood, 2012
Studies indicate that Macrophage-colony stimulating factor (CSF-1) signaling through its receptor (CSF-1R) promotes the differentiation of myeloid progenitors.
Microglial stimulation of glioblastoma invasion involves epidermal growth factor receptor (EGFR) and colony stimulating factor 1 receptor (CSF-1R) signaling.
Segall et al., New York City, United States. In Mol Med, 2011
Study results provide a mechanistic explanation for the involvement of CSF-1 in glioblastoma progression and indicate that inhibition of CSF-1R signaling could provide a novel approach to limiting glioblastoma invasion
Feedback inhibition of osteoclastogenesis during inflammation by IL-10, M-CSF receptor shedding, and induction of IRF8.
Takami et al., New York City, United States. In Ann N Y Acad Sci, 2011
In this review, shedding of macrophage-CSF receptor c-Fms inhibits osteoclastogenesis.
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